Heart failure

Heart failure (HF), often used to mean chronic heartfailure (CHF), occurs when the heart is unable to pumpsufficiently to maintain blood flow to meet the needsof the body.[1][2][3] The terms congestive heart failure(CHF) or congestive cardiac failure (CCF) are oftenused interchangeably with chronic heart failure.[4] Signsand symptoms commonly include shortness of breath,excessive tiredness, and leg swelling.[5] The shortness ofbreath is usually worse with exercise, when lying down,and at night while sleeping.[5] There is often a limitationon the amount of exercise people can perform, even whenwell treated.[6]

Common causes of heart failure include coronary arterydisease including a previous myocardial infarction (heartattack), high blood pressure, atrial fibrillation, valvularheart disease, and cardiomyopathy.[5][7] These causeheart failure by changing either the structure or the func-tioning of the heart.[5] There are two main types of heartfailure: heart failure due to left ventricular dysfunctionand heart failure with normal ejection fraction depend-ing on if the ability of the left ventricle to contract is af-fected, or the heart’s ability to relax.[5] The severity of dis-ease is usually graded by how much the ability to exerciseis decreased.[8] Heart failure is not the same as myocar-dial infarction (in which part of the heart muscle dies) orcardiac arrest (in which blood flow stops altogether).[9][10]Other diseases that may have symptoms similar to heartfailure include: obesity, kidney problems, liver problems,anemia and thyroid disease among others.[8]

The condition is diagnosed based on the historyof the symptoms and a physical examination withconfirmation by echocardiography.[11] Blood tests,electrocardiography, and chest radiography may beuseful to determine the underlying cause.[11] Treatmentdepends on the severity and cause of the disease.[11] Inpeople with chronic disease already in a stable situation,treatment commonly consists of lifestyle measuressuch as stopping smoking,[12] physical exercise,[13] anddietary changes, as well as medications.[12] In thosewith heart failure due to left ventricular dysfunction,angiotensin converting enzyme inhibitors and beta block-ers are recommended.[11] For those with severe disease,aldosterone antagonists, an angiotensin receptor blockeror hydralazine with a nitrate may be used.[11] If there isa normal ejection fraction, associated health problemsshould be treated.[11] Diuretics are useful for preventingfluid retention and thus recommended.[12] Sometimes,depending on the cause, an implanted device such asa pacemaker or implantable cardiac defibrillator may

be useful.[11] A ventricular assist device or occasionallya heart transplant may be recommended in those withsevere disease despite all other measures.[12]

Heart failure is a common, costly, and potentially fatalcondition.[7] In developed countries, around 2% of adultshave heart failure and in those over the age of 65, thisincreases to 6–10%.[7][14] In the year after diagnosis therisk of death is about 35% after which it decreases to be-low 10% each year.[5] This is similar to the risks witha number of types of cancer.[5] In the United Kingdomthe disease is the reason for 5% of emergent hospitaladmissions.[5] Heart failure has been known since ancienttimes with the Ebers papyrus commenting on it around1550 BCE.[6]

1 Terminology

Heart failure is a physiological state in which cardiac out-put is insufficient to meet the needs of the body and lungs.The termed “congestive heart failure” (CHF) is often usedas one of the common symptoms is swelling or waterretention.[15]

Heart failure is divided into two different types: heartfailure due to reduced ejection fraction (HFREF) alsoknown as heart failure due to left ventricular systolicdysfunction or systolic heart failure and heart failurewith preserved ejection fraction (HFPEF) also known asdiastolic heart failure or heart failure with normal ejectionfraction (HFNEF).[5][13] Heart failure with reduced ejec-tion fraction occurs when the ejection fraction is less than40%.[16] In diastolic heart failure, the heart muscle con-tracts well but the ventricle does not fill with blood wellin the relaxation phase.[5] Ejection fraction is the propor-tion of blood in the heart pumped out of the heart duringa single contraction.[17] It is a percentage with normal be-ing between 50 and 75%.[17]

The term “acute” is used to mean rapid onset, and“chronic” refers to long duration. Chronic heart fail-ure is a long term situation, usually with stable treatedsymptomatology. Acute decompensated heart failure isworsening or decompensated heart failure, referring toepisodes in which a person can be characterized as havinga change in heart failure signs and symptoms resulting ina need for urgent therapy or hospitalization.[18] Heart fail-ure may also occur in situations of “high output,” (termed"high output cardiac failure") where the ventricular sys-tolic function is normal but the heart cannot deal with an

1

2 2 SIGNS AND SYMPTOMS

important augmentation of blood volume.[19]

2 Signs and symptoms

A man with congestive heart failure and marked jugular venousdistension. External jugular vein marked by an arrow.

Heart failure symptoms are traditionally and somewhatarbitrarily divided into “left” and “right” sided, recogniz-ing that the left and right ventricles of the heart supplydifferent portions of the circulation. However, heart fail-ure is not exclusively backward failure (in the part of thecirculation which drains to the ventricle).There are several other exceptions to a simple left-rightdivision of heart failure symptoms. Additionally, themost common cause of right-sided heart failure is left-sided heart failure.[20] The result is that patients com-monly present with both sets of signs and symptoms.

2.1 Left-sided failure

Common respiratory signs are increased rate of breath-ing and increased work of breathing (non-specific signsof respiratory distress). Rales or crackles, heard initiallyin the lung bases, and when severe, throughout the lungfields suggest the development of pulmonary edema (fluidin the alveoli). Cyanosis which suggests severe hypox-emia, is a late sign of extremely severe pulmonary edema.Additional signs indicating left ventricular failure includea laterally displaced apex beat (which occurs if the heartis enlarged) and a gallop rhythm (additional heart sounds)

may be heard as a marker of increased blood flow, or in-creased intra-cardiac pressure. Heart murmurs may in-dicate the presence of valvular heart disease, either as acause (e.g. aortic stenosis) or as a result (e.g. mitral re-gurgitation) of the heart failure.Backward failure of the left ventricle causes congestionof the lungs’ blood vessels, and so the symptoms are pre-dominantly respiratory in nature. Backward failure canbe subdivided into failure of the left atrium, the left ven-tricle or both within the left circuit. The patient will havedyspnea (shortness of breath) on exertion and in severecases, dyspnea at rest. Increasing breathlessness on ly-ing flat, called orthopnea, occurs. It is often measuredin the number of pillows required to lie comfortably, andin orthopnea, the patient may resort to sleeping while sit-ting up. Another symptom of heart failure is paroxysmalnocturnal dyspnea: a sudden nighttime attack of severebreathlessness, usually several hours after going to sleep.Easy fatigability and exercise intolerance are also com-mon complaints related to respiratory compromise."Cardiac asthma" or wheezing may occur.Compromise of left ventricular forward function may re-sult in symptoms of poor systemic circulation such asdizziness, confusion and cool extremities at rest.

2.2 Right-sided failure

Physical examination may reveal pitting peripheraledema, ascites, and liver enlargement. Jugular venouspressure is frequently assessed as a marker of fluid sta-tus, which can be accentuated by eliciting hepatojugularreflux. If the right ventricular pressure is increased, aparasternal heave may be present, signifying the compen-satory increase in contraction strength.Backward failure of the right ventricle leads to conges-tion of systemic capillaries. This generates excess fluidaccumulation in the body. This causes swelling underthe skin (termed peripheral edema or anasarca) and usu-ally affects the dependent parts of the body first (causingfoot and ankle swelling in people who are standing up,and sacral edema in people who are predominantly ly-ing down). Nocturia (frequent nighttime urination) mayoccur when fluid from the legs is returned to the blood-stream while lying down at night. In progressively severecases, ascites (fluid accumulation in the abdominal cav-ity causing swelling) and liver enlargement may develop.Significant liver congestion may result in impaired liverfunction, and jaundice and even coagulopathy (problemsof decreased blood clotting) may occur.

2.3 Biventricular failure

Dullness of the lung fields to finger percussion and re-duced breath sounds at the bases of the lung may sug-gest the development of a pleural effusion (fluid collec-

3.2 Acute decompensation 3

tion in between the lung and the chest wall). Though itcan occur in isolated left- or right-sided heart failure, itis more common in biventricular failure because pleuralveins drain into both the systemic and pulmonary venoussystems. When unilateral, effusions are often right sided.

3 Causes

3.1 Congestive heart failure

Heart failure may also occur in situations of “highoutput,” (termed "high output cardiac failure") wherethe ventricular systolic function is normal but theheart cannot deal with an important augmentation ofblood volume.[19] This can occur in overload situation(blood or serum infusions), renal diseases, chronic se-vere anemia, beriberi (vitamin B1/thiamine deficiency),thyrotoxicosis, Paget’s disease, arteriovenous fistulae, orarteriovenous malformations.A study of healthy adults in the United States found thefollowing risk factors:[21]

1. Ischemic heart disease 62%

2. Cigarette smoking 16%

3. Hypertension (high blood pressure) 10%

4. Obesity 8%

5. Diabetes 3%

6. Valvular heart disease 2% (much higher in olderpopulations)

Italians had the following underlying causes:[22]

1. Ischemic heart disease 40%

2. Dilated cardiomyopathy 32%

3. Valvular heart disease 12%

4. Hypertension 11%

5. Other 5%

Rarer causes of heart failure include:

• Viral myocarditis (an infection of the heart muscle)

• Infiltrations of the muscle such as amyloidosis

• HIV cardiomyopathy (caused by human immunod-eficiency virus)

• Connective tissue diseases such as systemic lupuserythematosus

• Abuse of drugs such as alcohol and cocaine

• Pharmaceutical drugs such as chemotherapeuticagents

• Arrhythmias.

Obstructive sleep apnea (a condition of sleep whereindisordered breathing overlaps with obesity, hypertension,and/or diabetes) is regarded as an independent cause ofheart failure.

3.2 Acute decompensation

Main article: Acute decompensated heart failure

Chronic stable heart failure may easily decompensate.This most commonly results from an intercurrent illness(such as pneumonia), myocardial infarction (a heart at-tack), arrhythmias, uncontrolled hypertension, or a pa-tient’s failure to maintain a fluid restriction, diet, ormedication.[23] Other well recognized factors that mayworsen CHF include: anemia and hyperthyroidism whichplace additional strain on the heart muscle, excessive fluidor salt intake, and medication that causes fluid retentionsuch as NSAIDs and thiazolidinediones.[24] NSAIDs ingeneral increase the risk twofold.[25]

4 Pathophysiology

Heart failure is caused by any condition which reduces theefficiency of the myocardium, or heart muscle, throughdamage or overloading. As such, it can be caused by awide number of conditions, including myocardial infarc-tion (in which the heart muscle is starved of oxygen anddies), hypertension (which increases the force of contrac-tion needed to pump blood) and amyloidosis (in whichprotein is deposited in the heart muscle, causing it tostiffen). Over time these increases in workload will pro-duce changes to the heart itself:

• Reduced force of contraction, due to overloading ofthe ventricle. In a healthy heart, increased filling ofthe ventricle results in increased force of contraction(by the Frank–Starling law of the heart) and thus arise in cardiac output. In heart failure this mecha-nism fails, as the ventricle is loaded with blood to thepoint where heart muscle contraction becomes lessefficient. This is due to reduced ability to cross-linkactin and myosin filaments in over-stretched heartmuscle.[26]

• A reduced stroke volume, as a result of a failure ofsystole, diastole or both. Increased end systolic vol-ume is usually caused by reduced contractility. De-creased end diastolic volume results from impairedventricular filling – as occurs when the complianceof the ventricle falls (i.e. when the walls stiffen).

4 4 PATHOPHYSIOLOGY

• Reduced spare capacity. As the heart works harderto meet normal metabolic demands, the amount car-diac output can increase in times of increased oxy-gen demand (e.g. exercise) is reduced. This con-tributes to the exercise intolerance commonly seenin heart failure. This translates to the loss of one’scardiac reserve, or the ability of the heart to workharder during strenuous physical activity. Sincethe heart has to work harder to meet the normalmetabolic demands, it is incapable of meeting themetabolic demands of the body during exercise.

• Increased heart rate, stimulated by increased sym-pathetic activity[27] in order to maintain cardiac out-put. Initially, this helps compensate for heart fail-ure bymaintaining blood pressure and perfusion, butplaces further strain on the myocardium, increasingcoronary perfusion requirements, which can lead toworsening of ischemic heart disease. Sympatheticactivity may also cause potentially fatal arrhythmias.

• Hypertrophy (an increase in physical size) of themyocardium, caused by the terminally differenti-ated heart muscle fibres increasing in size in an at-tempt to improve contractility. This may contributeto the increased stiffness and decreased ability to re-lax during diastole.

• Enlargement of the ventricles, contributing to theenlargement and spherical shape of the failing heart.The increase in ventricular volume also causes a re-duction in stroke volume due to mechanical and in-efficient contraction of the heart.[28]

The general effect is one of reduced cardiac output andincreased strain on the heart. This increases the risk ofcardiac arrest (specifically due to ventricular dysrhyth-mias), and reduces blood supply to the rest of the body. Inchronic disease the reduced cardiac output causes a num-ber of changes in the rest of the body, some of which arephysiological compensations, some of which are part ofthe disease process:

• Arterial blood pressure falls. This destimulatesbaroreceptors in the carotid sinus and aortic archwhich link to the nucleus tractus solitarii. This cen-ter in the brain increases sympathetic activity, re-leasing catecholamines into the blood stream. Bind-ing to alpha-1 receptors results in systemic arterialvasoconstriction. This helps restore blood pressurebut also increases the total peripheral resistance, in-creasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heartrate and make contractions more forceful, in an at-tempt to increase cardiac output. This also, how-ever, increases the amount of work the heart has toperform.

• Increased sympathetic stimulation also causes theposterior pituitary to secrete vasopressin (also

known as antidiuretic hormone or ADH), whichcauses fluid retention at the kidneys. This increasesthe blood volume and blood pressure.

• Reduced perfusion (blood flow) to the kidneys stim-ulates the release of renin – an enzyme whichcatalyses the production of the potent vasopressorangiotensin. Angiotensin and its metabolites causefurther vasoconstriction, and stimulate increased se-cretion of the steroid aldosterone from the adrenalglands. This promotes salt and fluid retention at thekidneys.

• The chronically high levels of circulating neu-roendocrine hormones such as catecholamines,renin, angiotensin, and aldosterone affects the my-ocardium directly, causing structural remodelling ofthe heart over the long term. Many of these re-modelling effects seem to be mediated by trans-forming growth factor beta (TGF-beta), which is acommon downstream target of the signal transduc-tion cascade. initiated by catecholamines[29] and an-giotensin II,[30] and also by epidermal growth factor(EGF), which is a target of the signaling pathwayactivated by aldosterone[31]

• Reduced perfusion of skeletal muscle causes atrophyof the muscle fibres. This can result in weakness,increased fatigueability and decreased peak strength– all contributing to exercise intolerance.[32]

The increased peripheral resistance and greater blood vol-ume place further strain on the heart and accelerates theprocess of damage to the myocardium. Vasoconstrictionand fluid retention produce an increased hydrostatic pres-sure in the capillaries. This shifts the balance of forcesin favour of interstitial fluid formation as the increasedpressure forces additional fluid out of the blood, into thetissue. This results in edema (fluid build-up) in the tis-sues. In right-sided heart failure this commonly starts inthe ankles where venous pressure is high due to the effectsof gravity (although if the patient is bed-ridden, fluid ac-cumulation may begin in the sacral region.) It may alsooccur in the abdominal cavity, where the fluid build-up iscalled ascites. In left-sided heart failure edema can occurin the lungs – this is called cardiogenic pulmonary edema.This reduces spare capacity for ventilation, causes stiff-ening of the lungs and reduces the efficiency of gas ex-change by increasing the distance between the air and theblood. The consequences of this are dyspnea (shortnessof breath), orthopnea and paroxysmal nocturnal dyspnea.The symptoms of heart failure are largely determined bywhich side of the heart fails. The left side pumps bloodinto the systemic circulation, whilst the right side pumpsblood into the pulmonary circulation. Whilst left-sidedheart failure will reduce cardiac output to the systemiccirculation, the initial symptoms often manifest due toeffects on the pulmonary circulation. In systolic dysfunc-tion, the ejection fraction is decreased, leaving an abnor-

4.2 Diastolic dysfunction 5

mally elevated volume of blood in the left ventricle. In di-astolic dysfunction, end-diastolic ventricular pressure willbe high. This increase in volume or pressure backs up tothe left atrium and then to the pulmonary veins. Increasedvolume or pressure in the pulmonary veins impairs thenormal drainage of the alveoli and favors the flow of fluidfrom the capillaries to the lung parenchyma, causing pul-monary edema. This impairs gas exchange. Thus, left-sided heart failure often presents with respiratory symp-toms: shortness of breath, orthopnea and paroxysmalnocturnal dyspnea.In severe cardiomyopathy, the effects of decreased car-diac output and poor perfusion become more apparent,and patients will manifest with cold and clammy extrem-ities, cyanosis, claudication, generalized weakness, dizzi-ness, and syncope.The resultant hypoxia caused by pulmonary edema causesvasoconstriction in the pulmonary circulation, which re-sults in pulmonary hypertension. Since the right ventri-cle generates far lower pressures than the left ventricle(approximately 20 mmHg versus around 120 mmHg, re-spectively, in the healthy individual) but nonetheless gen-erates cardiac output exactly equal to the left ventricle,this means that a small increase in pulmonary vascularresistance causes a large increase in amount of work theright ventricle must perform. However, the main mech-anism by which left-sided heart failure causes right-sidedheart failure is actually not well understood. Some theo-ries invoke mechanisms that are mediated by neurohor-monal activation.[33] Mechanical effects may also con-tribute. As the left ventricle distends, the intraventric-ular septum bows into the right ventricle, decreasing thecapacity of the right ventricle.

4.1 Systolic dysfunction

Heart failure caused by systolic dysfunction is more read-ily recognized. It can be simplistically described as fail-ure of the pump function of the heart. It is character-ized by a decreased ejection fraction (less than 45%). Thestrength of ventricular contraction is attenuated and inad-equate for creating an adequate stroke volume, resultingin inadequate cardiac output. In general, this is caused bydysfunction or destruction of cardiac myocytes or theirmolecular components. In congenital diseases such asDuchenne muscular dystrophy, the molecular structureof individual myocytes is affected. Myocytes and theircomponents can be damaged by inflammation (such asin myocarditis) or by infiltration (such as in amyloido-sis). Toxins and pharmacological agents (such as ethanol,cocaine, doxorubicin, and amphetamines) cause intracel-lular damage and oxidative stress. The most commonmechanism of damage is ischemia causing infarction andscar formation. After myocardial infarction, dead my-ocytes are replaced by scar tissue, deleteriously affectingthe function of the myocardium. On echocardiogram,this is manifest by abnormal wall motion (hypokinesia)

or absent wall motion (akinesia).Because the ventricle is inadequately emptied, ventricu-lar end-diastolic pressure and volumes increase. This istransmitted to the atrium. On the left side of the heart,the increased pressure is transmitted to the pulmonaryvasculature, and the resultant hydrostatic pressure favorsextravasation of fluid into the lung parenchyma, causingpulmonary edema. On the right side of the heart, the in-creased pressure is transmitted to the systemic venous cir-culation and systemic capillary beds, favoring extravasa-tion of fluid into the tissues of target organs and extrem-ities, resulting in dependent peripheral edema.

4.2 Diastolic dysfunction

Heart failure caused by diastolic dysfunction is gener-ally described as the failure of the ventricle to ade-quately relax and typically denotes a stiffer ventricularwall. This causes inadequate filling of the ventricle, andtherefore results in an inadequate stroke volume. Thefailure of ventricular relaxation also results in elevatedend-diastolic pressures, and the end result is identical tothe case of systolic dysfunction (pulmonary edema in leftheart failure, peripheral edema in right heart failure).Diastolic dysfunction can be caused by processes simi-lar to those that cause systolic dysfunction, particularlycauses that affect cardiac remodeling.Diastolic dysfunction may not manifest itself except inphysiologic extremes if systolic function is preserved.The patient may be completely asymptomatic at rest.However, they are exquisitely sensitive to increases inheart rate, and sudden bouts of tachycardia (which canbe caused simply by physiological responses to exertion,fever, or dehydration, or by pathological tachyarrhyth-mias such as atrial fibrillation with rapid ventricular re-sponse) may result in flash pulmonary edema. Adequaterate control (usually with a pharmacological agent thatslows down AV conduction such as a calcium channelblocker or a beta-blocker) is therefore key to preventingdecompensation.Left ventricular diastolic function can be determinedthrough echocardiography bymeasurement of various pa-rameters such as the E/A ratio (early-to-atrial left ven-tricular filling ratio), the E (early left ventricular filling)deceleration time, and the isovolumic relaxation time.

5 Diagnosis

No system of diagnostic criteria has been agreed as thegold standard for heart failure. The National Institutefor Health and Care Excellence recommends a measur-ing brain natriuretic peptide followed by ultrasound of theheart if positive.[34]

6 5 DIAGNOSIS

Acute pulmonary edema. Note enlarged heart size, apical vascu-lar redistribution ( circle ), and small bilateral pleural effusions( arrow ).

5.1 Imaging

Echocardiography is commonly used to support a clinicaldiagnosis of heart failure. This modality uses ultrasoundto determine the stroke volume (SV, the amount of bloodin the heart that exits the ventricles with each beat), theend-diastolic volume (EDV, the total amount of bloodat the end of diastole), and the SV in proportion to theEDV, a value known as the ejection fraction (EF). In pe-diatrics, the shortening fraction is the preferred measureof systolic function. Normally, the EF should be be-tween 50% and 70%; in systolic heart failure, it dropsbelow 40%. Echocardiography can also identify valvularheart disease and assess the state of the pericardium (theconnective tissue sac surrounding the heart). Echocar-diography may also aid in deciding what treatments willhelp the patient, such as medication, insertion of animplantable cardioverter-defibrillator or cardiac resyn-chronization therapy. Echocardiography can also helpdetermine if acute myocardial ischemia is the precipi-tating cause, and may manifest as regional wall motionabnormalities on echo.Chest X-rays are frequently used to aid in the diagnosisof CHF. In a person who is compensated, this may showcardiomegaly (visible enlargement of the heart), quanti-fied as the cardiothoracic ratio (proportion of the heartsize to the chest). In left ventricular failure, there maybe evidence of vascular redistribution (“upper lobe blooddiversion” or “cephalization”), Kerley lines, cuffing of theareas around the bronchi, and interstitial edema. Ul-trasound of the lung may also be able to detect Kerleylines.[35]

5.2 Electrophysiology

An electrocardiogram (ECG/EKG) may be used to iden-tify arrhythmias, ischemic heart disease, right and left

ventricular hypertrophy, and presence of conduction de-lay or abnormalities (e.g. left bundle branch block). Al-though these findings are not specific to the diagnosis ofheart failure a normal ECG virtually excludes left ventric-ular systolic dysfunction.[36]

5.3 Blood tests

Blood tests routinely performed include electrolytes(sodium, potassium), measures of renal function, liverfunction tests, thyroid function tests, a complete bloodcount, and often C-reactive protein if infection is sus-pected. An elevated B-type natriuretic peptide (BNP) isa specific test indicative of heart failure. Additionally,BNP can be used to differentiate between causes of dys-pnea due to heart failure from other causes of dyspnea. Ifmyocardial infarction is suspected, various cardiac mark-ers may be used.According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heartfailure, BNP is a better indicator for heart failure andleft ventricular systolic dysfunction. In groups of symp-tomatic patients, a diagnostic odds ratio of 27 for BNPcompares with a sensitivity of 85% and specificity of 84%in detecting heart failure.[37]

5.4 Angiography

Heart failure may be the result of coronary artery dis-ease, and its prognosis depends in part on the ability ofthe coronary arteries to supply blood to the myocardium(heart muscle). As a result, coronary catheterizationmay be used to identify possibilities for revascularisationthrough percutaneous coronary intervention or bypasssurgery.

5.5 Monitoring

Various measures are often used to assess the progressof patients being treated for heart failure. These includefluid balance (calculation of fluid intake and excretion),monitoring body weight (which in the shorter term re-flects fluid shifts).[38]

5.6 Classification

There are many different ways to categorize heart failure,including:

• the side of the heart involved (left heart failure ver-sus right heart failure). Right heart failure compro-mises pulmonary flow to the lungs. Left heart fail-ure compromises aortic flow to the body and brain.Mixed presentations are common; left heart failureoften leads to right heart failure in the longer term.

5.7 Algorithms 7

• whether the abnormality is due to insufficientcontraction (systolic dysfunction), or due to insuffi-cient relaxation of the heart (diastolic dysfunction),or to both.

• whether the problem is primarily increased venousback pressure (preload), or failure to supply ade-quate arterial perfusion (afterload).

• whether the abnormality is due to low cardiac outputwith high systemic vascular resistance or high car-diac output with low vascular resistance (low-outputheart failure vs. high-output heart failure).

• the degree of functional impairment conferred bythe abnormality (as reflected in the New York HeartAssociation Functional Classification[39])

• the degree of coexisting illness: i.e. heart fail-ure/systemic hypertension, heart failure/pulmonaryhypertension, heart failure/diabetes, heart fail-ure/kidney failure, etc.

Functional classification generally relies on the New YorkHeart Association functional classification. The classes(I-IV) are:

• Class I: no limitation is experienced in any activities;there are no symptoms from ordinary activities.

• Class II: slight, mild limitation of activity; the patientis comfortable at rest or with mild exertion.

• Class III: marked limitation of any activity; the pa-tient is comfortable only at rest.

• Class IV: any physical activity brings on discomfortand symptoms occur at rest.

This score documents severity of symptoms, and can beused to assess response to treatment. While its use iswidespread, the NYHA score is not very reproducible anddoes not reliably predict the walking distance or exercisetolerance on formal testing.[40]

In its 2001 guidelines the American College of Cardi-ology/American Heart Association working group intro-duced four stages of heart failure:[41]

• Stage A: Patients at high risk for developing HF inthe future but no functional or structural heart dis-order.

• Stage B: a structural heart disorder but no symptomsat any stage.

• Stage C: previous or current symptoms of heart fail-ure in the context of an underlying structural heartproblem, but managed with medical treatment.

• Stage D: advanced disease requiring hospital-basedsupport, a heart transplant or palliative care.

The ACC staging system is useful in that Stage A en-compasses “pre-heart failure” – a stage where interven-tion with treatment can presumably prevent progressionto overt symptoms. ACC Stage A does not have a corre-sponding NYHA class. ACC Stage B would correspondto NYHA Class I. ACC Stage C corresponds to NYHAClass II and III, while ACC Stage D overlaps with NYHAClass IV.

5.7 Algorithms

There are various algorithms for the diagnosis of heartfailure. For example, the algorithm used by theFramingham Heart Study adds together criteria mainlyfrom physical examination. In contrast, the more ex-tensive algorithm by the European Society of Cardiol-ogy (ESC) weights the difference between supporting andopposing parameters from the medical history, physicalexamination, further medical tests as well as response totherapy.

5.7.1 Framingham criteria

By the Framingham criteria, diagnosis of congestiveheart failure (heart failure with impaired pumpingcapability)[15] requires the simultaneous presence of atleast 2 of the following major criteria or 1 major criterionin conjunction with 2 of the following minor criteria:Major criteria include the following:[42]

• Cardiomegaly on chest radiography

• S3 gallop (a third heart sound)

• Acute pulmonary edema

• Paroxysmal nocturnal dyspnea

• Crackles on lung auscultation

• Central venous pressure of more than 16 cm H2O at the right atrium

• Jugular vein distension

• Positive abdominojugular test

• Weight loss of more than 4.5 kg in 5 days in re-sponse to treatment (sometimes classified as a minorcriterion[43])

Minor criteria include the following:[42]

• Tachycardia of more than 120 beats per minute

• Nocturnal cough

• Dyspnea on ordinary exertion

• Pleural effusion

8 6 MANAGEMENT

• Decrease in vital capacity by one third from maxi-mum recorded

• Hepatomegaly

• Bilateral ankle edema

Minor criteria are acceptable only if they can not be at-tributed to another medical condition such as pulmonaryhypertension, chronic lung disease, cirrhosis, ascites,or the nephrotic syndrome.[42] The Framingham HeartStudy criteria are 100% sensitive and 78% specificfor identifying persons with definite congestive heartfailure.[42]

5.7.2 ESC algorithm

The ESC algorithm weights the following parameters inestablishing the diagnosis of heart failure:[44]

5.8 Differential diagnosis

There are several terms which are closely related to heartfailure, and may be the cause of heart failure, but shouldnot be confused with it:

• Cardiac arrest and asystole refer to situations inwhich there is no cardiac output at all. Without ur-gent treatment these result in sudden death.

• Myocardial infarction (“Heart attack”) refers toheart muscle damage due to insufficient blood sup-ply, usually as a result of a blocked coronary artery.

• Cardiomyopathy refers specifically to problemswithin the heart muscle, and these problems can re-sult in heart failure. Ischemic cardiomyopathy im-plies that the cause of muscle damage is coronaryartery disease. Dilated cardiomyopathy implies thatthe muscle damage has resulted in enlargement ofthe heart. Hypertrophic cardiomyopathy involvesenlargement and thickening of the heart muscle.

6 Management

Main article: Management of heart failure

Treatment focuses on improving the symptoms and pre-venting the progression of the disease. Reversiblecauses of the heart failure also need to be addressed(e.g. infection, alcohol ingestion, anemia, thyrotoxicosis,arrhythmia, hypertension). Treatments include lifestyleand pharmacological modalities, and occasionally vari-ous forms of device therapy and rarely cardiac transplan-tation.

6.1 Acute decompensation

Main article: Acute decompensated heart failure

In acute decompensated heart failure (ADHF), the im-mediate goal is to re-establish adequate perfusion andoxygen delivery to end organs. This entails ensuringthat airway, breathing, and circulation are adequate. Im-mediate treatments usually involve some combinationof vasodilators such as nitroglycerin, diuretics such asfurosemide, and possibly non invasive positive pressureventilation (NIPPV).

6.2 Chronic management

The goal of treatment in those with chronic heart fail-ure is the prevention of acute decompensation, to coun-teract the deleterious effects of cardiac remodeling, andto minimize the symptoms. First-line therapy for allpeople with heart failure due to reduced systolic func-tion is angiotensin-converting enzyme (ACE) inhibitors.Medicines from this class improve survival and qual-ity of life in those with heart failure.[45] Furthermore,medicines from the beta blocker class have been asso-ciated with similar improvement in mortality and symp-toms, and are also recommended.[45] The mortality ben-efits of beta blockers in people with systolic dysfunctionwho also have atrial fibrillation (AF) is more limited thanin those who do not have AF.[46] If the ejection fractionis not dimished (HFPEF), the benefits of beta blockers ismore modest; a decrease in mortality has been observedbut no reduction in hospital admission for uncontrolledsymptoms.[47]

Diuretics have been a mainstay of treatment for treat-ment of fluid accumulation, and include classes of di-uretics such as loop diuretics, thiazide-like diuretic, andpotassium-sparing diuretic. Although widely used, ev-idence on their efficacy and safety is limited.[48] A re-cent Cochrane review found in a small studies, individualswith heart failure taking diuretics appeared to have im-proved mortality.[49] However, the extent to which theseresults can be extrapolated to a general population is un-clear due to the small number of participants in the citedstudies.[48]

In addition to pharmacologic agents (oral loop diuret-ics, beta-blockers, ACE inhibitors or angiotensin recep-tor blockers, vasodilators, and in severe cardiomyopathyaldosterone receptor antagonists), behavioral modifica-tion should be pursued, specifically with regard to dietaryguidelines regarding fluid intake.Exercise should be encouraged as tolerated, as sufficientconditioning can significantly improve quality of life andreduce the risk of hospital admission for worsening symp-toms. No benefit in mortality has been found for exercise.It is not clear if the evidence can be extended to peoplewith HFPEF, and to when the exercise takes place en-

9

tirely at home.[50]

Anemia is an independent factor in mortality in peoplewith chronic heart failure; treatment of anemia signifi-cantly improves quality of life for those with heart fail-ure, and has been shown to improve the classification ofseverity of heart failure.[51] Treatment of anaemia im-proves quality of life and decreases mortality rates.[52]Due to this increasing evidence, the latest Europeanguidelines recommend screening for anaemia and treat-ing with parenteral iron if anaemia is found.[53]

In people with severe cardiomyopathy (left ventricu-lar ejection fraction below 35%), implantation of anautomatic implantable cardioverter defibrillator (AICD)should be considered to reduce the risk of severe life-threatening arrhythmias. A select population (LVEF<35% and evidence of abnormal conduction on ECGor echocardiogram) will also probably benefit fromventricular resynchronization.[54] In select cases, cardiactransplantation can be considered. While this may resolvethe problems associated with heart failure, the persongenerally must remain on an immunosuppressive regimento prevent rejection, which has its own significant down-sides. Some people with heart failure may also be can-didates for ventricular assist devices (VAD), which havecommonly been used as a bridge to heart transplants, butare also now being used as treatments for very advancedheart failure in certain people even if transplantation willnot be offered.[55]

Home visits and heart failure clinic have been found to bebeneficial with respect to need for hospitalization and lifeexpectancy.[56]

6.3 Palliative care

People with CHF often have significant symptoms, suchas shortness of breath and chest pain. Both palliative careand cardiology are trying to get palliative care involvedearlier in the course of patients with heart failure, andsome would argue any patient with NYHA class III CHFshould have a palliative care referral. Palliative care cannot only provide symptom management, but also assistwith advanced care planning, goals of care in the caseof a significant decline, and making sure the patient has amedical power of attorney and discussed his or her wisheswith this individual.[57]

Without transplantation, heart failure may not be re-versible and cardiac function typically deteriorates withtime. The growing number of patients with Stage IV heartfailure (intractable symptoms of fatigue, shortness ofbreath or chest pain at rest despite optimal medical ther-apy) should be considered for palliative care or hospice,according to American College of Cardiology/AmericanHeart Association guidelines.[57]

7 Prognosis

Prognosis in heart failure can be assessed inmultiple waysincluding clinical prediction rules and cardiopulmonaryexercise testing. Clinical prediction rules use a compos-ite of clinical factors such as lab tests and blood pressureto estimate prognosis. Among several clinical predictionrules for prognosing acute heart failure, the 'EFFECTrule' slightly outperformed other rules in stratifying pa-tients and identifying those at low risk of death duringhospitalization or within 30 days.[58] Easy methods foridentifying low risk patients are:

• ADHERE Tree rule indicates that patients withblood urea nitrogen < 43 mg/dl and systolic bloodpressure at least 115 mm Hg have less than 10%chance of inpatient death or complications.

• BWH rule indicates that patients with systolic bloodpressure over 90 mm Hg, respiratory rate of 30 orless breaths per minute, serum sodium over 135mmol/L, no new ST-T wave changes have less than10% chance of inpatient death or complications.

A very important method for assessing prognosis in ad-vanced heart failure patients is cardiopulmonary exercisetesting (CPX testing). CPX testing is usually requiredprior to heart transplantation as an indicator of progno-sis. Cardiopulmonary exercise testing involves measure-ment of exhaled oxygen and carbon dioxide during ex-ercise. The peak oxygen consumption (VO2 max) isused as an indicator of prognosis. As a general rule, aVO2 max less than 12–14 cc/kg/min indicates a poorsurvival and suggests that the patient may be a candi-date for a heart transplant. Patients with a VO2 max<10cc/kg/min have clearly poorer prognosis. Themost recentInternational Society for Heart and Lung Transplantation(ISHLT) guidelines[59] also suggest two other parametersthat can be used for evaluation of prognosis in advancedheart failure, the heart failure survival score and the useof a criterion of VE/VCO2 slope > 35 from the CPX test.The heart failure survival score is a score calculated us-ing a combination of clinical predictors and the VO2maxfrom the cardiopulmonary exercise test.Heart failure is associated with significantly reducedphysical and mental health, resulting in a markedly de-creased quality of life.[60][61] With the exception of heartfailure caused by reversible conditions, the condition usu-ally worsens with time. Although some people survivemany years, progressive disease is associated with anoverall annual mortality rate of 10%.[62]

8 Epidemiology

Heart failure is associated with a high health expenditure,mostly because of the cost of hospitalizations; costs have

10 11 REFERENCES

been estimated to amount to 2% of the total budget ofthe National Health Service in the United Kingdom, andmore than $35 billion in the United States.[63][64]

Heart failure is the leading cause of hospitalization inpeople older than 65.[65] In developed countries, themeanage of patients with heart failure is 75 years old. In de-veloping countries, two to three percent of the populationhave heart failure, but in those 70 to 80 years old, it oc-curs in 20–30 percent.More than 20 million people have heart failureworldwide.[66][67] The prevalence and incidence of heartfailure are increasing, mostly because of increasinglife span, but also because of increased prevalence ofrisk factors (hypertension, diabetes, dyslipidemia, andobesity) and improved survival rates from other types ofcardiovascular disease (myocardial infarction, valvulardisease, and arrhythmias).[67][68]

In the United States, heart failure affects 5.8 million peo-ple, and each year 550,000 new cases are diagnosed.[66]In 2011, congestive heart failure was the most com-mon reason for hospitalization for adults aged 85 yearsand older, and the second most common for adults aged65–84 years.[69] Heart failure is much higher in AfricanAmericans, Hispanics, Native Americans and recent im-migrants from the eastern bloc countries like Russia. Thishigh prevalence in these ethnic minority populations hasbeen linked to high incidence of diabetes and hyperten-sion. In many new immigrants to the U.S., the high preva-lence of heart failure has largely been attributed to lackof preventive health care or substandard treatment.[70]Nearly one out of every four patients (24.7%) hospital-ized in the U.S. with congestive heart failure are readmit-ted within 30 days.[71] Additionally, more than 50% ofpatients seek re-admission within 6 months after treat-ment and the average duration of hospital stay is 6 days.In tropical countries, the most common cause of HF isvalvular heart disease or some type of cardiomyopathy.As underdeveloped countries have become more afflu-ent, there has also been an increase in the incidence ofdiabetes, hypertension and obesity, which have in turnraised the incidence of heart failure.[72]

Congestive heart failure is a leading cause of hospitalreadmissions in the U.S. In a study of 18 States, Medi-care patients aged 65 and older were readmitted at a rateof 24.5 per 100 admissions in 2011. In the same year,Medicaid patients were readmitted at a rate of 30.4 per100 admissions, and uninsured patients were readmittedat a rate of 16.8 per 100 admissions. These are the high-est readmission rates for both patient categories. Notably,congestive heart failure was not among the top ten condi-tions with the most 30-day readmissions among the pri-vately insured.[73]

8.1 Sex

Men have a higher incidence of heart failure, but the over-all prevalence rate is similar in both sexes, since womensurvive longer after the onset of heart failure.[74] Womentend to be older when diagnosed with heart failure (aftermenopause), they are more likely than men to have dias-tolic dysfunction, and seem to experience a lower overallquality of life than men after diagnosis.[74]

9 Economics

In 2011, non-hypertensive congestive heart failure wasone of the ten most expensive conditions seen during in-patient hospitalizations in the U.S., with aggregate inpa-tient hospital costs of more than $10.5 billion.[75]

10 Research

There is low quality evidence that stem cell therapy mayhelp.[76] Although this evidence positively indicated ben-efit, the evidence was of lower quality than other evidencethat does not indicate benefit.[77]

A previous claim, which came from a 2012 article pub-lished by the British Journal Heart, stated that a low saltdiet increased the risk of death in those with congestiveheart failure. This claim has since been withdrawn. Thepaper was retracted by the journal in 2013 because two ofthe cited studies contained duplicate data that could notbe verified, and the data has since been lost.[78][79][80]

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12 External links• Heart failure, American Heart Association – infor-mation and resources for treating and living withheart failure

• Heart Failure Matters – patient information websiteof the Heart Failure Association of the EuropeanSociety of Cardiology

• Heart failure in children by Great Ormond StreetHospital, London, UK

15

13 Text and image sources, contributors, and licenses

13.1 Text• Heart failure Source: http://en.wikipedia.org/wiki/Heart%20failure?oldid=644660996 Contributors: Bryan Derksen, The Anome,

Alex.tan, Danny, Stevertigo, Edward, Karada, Ahoerstemeier, Ronz, Kingturtle, Александър, Julesd, Cratbro, Selket, Topbanana, Chu-unen Baka, Altenmann, Nurg, Spin2cool, Hadal, Kd4ttc, Giftlite, DocWatson42, Techelf, Ksheka, Tarek, Bork, Curps, Niteowlneils,Jfdwolff, Hugh2414, Jmmurphy, Theblog, Gscshoyru, Neutrality, Kate, Mike Rosoft, Discospinster, Rich Farmbrough, Bender235, ESkog,Mr. Billion, El C, Smalljim, Davidruben, Arcadian, Kbir1, Merope, Alansohn, Wouterstomp, Axl, Bart133, Wiccan Quagga, Club-marx, Versageek, SteinbDJ, CoolMike, Woohookitty, Lunar Jesters, Uncle G, Benbest, Eras-mus, Graham87, BD2412, Jclemens, Cander-son7, Rjwilmsi, Rschen7754, RobertG, Nihiltres, Stevenfruitsmaak, Dexcel, Roboto de Ajvol, YurikBot, Stephenb, Eleassar, Rsrikanth05,NawlinWiki, Aeusoes1, Grafen, Joel7687, Nephron, Supten, Saintamh, Andrewr47, Nescio, IceCreamAntisocial, Jacklee, Closedmouth,Badgettrg, Höyhens, Allens, Aswang, Tom Morris, SmackBot, Limnestor, Bigbluefish, Rachel Pearce, Ohnoitsjamie, Skizzik, Oskarpear-son, Maatsby, Atrzcins, Bluebot, MikeSy, RDBrown, Oli Filth, MalafayaBot, Uthbrian, Dlohcierekim’s sock, DHN-bot, Scwlong, Awolf1,SheeEttin, Chwats, Chlewbot, KaiserbBot, Rrburke, Zvar, Laban712, Atomskninja, Andrew c, Jklin, SalopianJames, Vanished user 9i39j3,John, Scientizzle, Rossodio, Sir Nicholas de Mimsy-Porpington, Beetstra, Kyoko, Cajolingwilhelm, InedibleHulk, Daviddaniel37, Shak-ingSpirit, Hu12, Gnusmas, Fvasconcellos, CmdrObot, Unionhawk, Megaboz, The Font, Leevanjackson, Im.a.lumberjack, DanielRigal,Meodipt, JVinocur, Clappingsimon, Fafabifiofo, Christian75, The1anton, Unclfester, JamesAM, Joncomelately, Headbomb, Cool Blue,Nick Number, Dawnseeker2000, CowardX10, Thadius856, Cyclonenim, Milton Stanley, Cwray, Tlabshier, Dan D. Ric, Barek, MER-C,Db099221, Acroterion, Magioladitis, Bongwarrior, DMY, WhatamIdoing, Mrpulley, Schaddm, DerHexer, Yobol, Hdt83, STBot, Ret-tetast, TheEgyptian, D Dinneen, LedgendGamer, J.delanoy, VELVET, RadioGuyTed, Nbauman, Zizanie13, Jeyradan, Enuja, Nemobis, Mergneed, Mikael Häggström, Danjeffers, Toanke, Tommedici, Aaron Walkhouse, CWii, Msrocha, Hersfold, Almazi, Badgerzilla,Natyrrr, Dwight666, Gwib, A4bot, Ann Stouter, Don4of4, LeaveSleaves, PDFbot, BotKung, Epgui, DebbieV76, Gebbiegirl, Falcon8765,Brianga, HeirloomGardener, Countincr, Doc James, AlleborgoBot, JustinMullins, SieBot, Vcamyv, Hertz1888, Alexisfan, Geniuskyle,BService, LeadSongDog, Thesavagenorwegian, Hosim, Bobjgalindo, Ddnile, Khvalamde, KathrynLybarger, Vikram.d.singh, 9eyedeel,Mike2vil, Good2Bherewithyou, Tenacious.doc, Denisarona, Martarius, Animeronin, ClueBot, LAX, Kafka Liz, Anta111, Sailormd, MildBill Hiccup, Uncle Milty, Findfunds, Aqua lem, Lbeben, Ottawahitech, Lbertolotti, DragonBot, Excirial, Alexbot, Ykhwong, Arjayay,Dekisugi, Rustamabd, Edwiki25, Thebagman, Dana boomer, Johnuniq, SoxBot III, Jlf64, RexxS, XLinkBot, MarmotteNZ, NellieBly,TamePhysician, Addbot, Glangmann, DOI bot, Elvire, Fyrael, Aojinglu, CanadianLinuxUser, Diptanshu.D, Jpoelma13, Jim10701, Phar-aclipper, LinkFA-Bot, Tide rolls, Lightbot, Zjahna, आशीष भटनागर, Yobot, Beeswaxcandle, Frostie Jack, KamikazeBot, Mspowell134,Langthorne, AnomieBOT, Jim1138, Salte013, Nhy67ygv, Jo3sampl, Bluerasberry, Materialscientist, April13salix, Citation bot, Jmarchn,Michael Chidester, Jeffrey Mall, Acebulf, Foszto, Srich32977, Ruy Pugliesi, GrouchoBot, SciberDoc, Dr.satan257, Maria Sieglinda vonNudeldorf, Kyng, Medic2008, ChillyMD, Doc4health, Sanecare, Joaquin008, Patelht, Ramonbover, FrescoBot, LuisArmandoRasteletti,VFDA, BoundaryRider, HamburgerRadio, Citation bot 1, Redrose64, Pinethicket, Acurx, Jonesey95, Tinton5, Orangeroof, Pbsouth-wood, Jhbuk, Llevanloc, Anim8cme, Trappist the monk, Animalparty, Tofutwitch11, Afr77, HCUP US, Vrenator, Paiamshadi, Terry-firma, Tbhotch, Samozaparola, The Legendary Sky Attacker, RjwilmsiBot, Thomase89, EmausBot, John of Reading, Lucien504, Rjparks,Shaanon, Dcirovic, Thecheesykid, Crise Cardiaque, AManWithNoPlan, Chattanoogadoc, Anupamgahalout, E. Fokker, Helpsome, Clue-Bot NG, Hon-3s-T, Wimpus, MaHealthy03, Widr, Panterdjuret, Telpardec, Syleth, Guptan99, MerlIwBot, Waiors, Belton1, Curb Chain,Smb1217, Storey246, RichNelson, Cstorr09, Sahara4u, Mudcathi, Naivepanda, Beatlemania159, Barroso123, Wikitorrens, Bijaykm21,Glacialfox, LindaFisher7, Kidneyman47, Rytyho usa, Om.Tem, BattyBot, Deviceman, Randantor, ChrisGualtieri, YFdyh-bot, TylerDur-den8823, JesseAlanGordon, Dexbot, Fahd hk25, SoledadKabocha, Rory 20 uk, MichaelJones7141, Makecat-bot, Sandrock2242, DocElisa,Chantal Cooper, Faizan, Rpzrz, Iztwoz, Bbbfn, Dozzzzzzzzzing off, Alice Person, Josepaulopineda, Ojbooker, Anrnusna, Krayonbox, Cyril-lec, Profmawk, Monkbot, LegoFan506, ConeyBearHug, Tooth10, Vinit J and Anonymous: 467

13.2 Images• File:Commons-logo.svg Source: http://upload.wikimedia.org/wikipedia/en/4/4a/Commons-logo.svg License: ? Contributors: ? Originalartist: ?

• File:Elevated_JVP.JPG Source: http://upload.wikimedia.org/wikipedia/commons/4/4d/Elevated_JVP.JPG License: CC BY-SA 3.0Contributors: Own work Original artist: James Heilman, MD

• File:Pulmonaryedema09.JPG Source: http://upload.wikimedia.org/wikipedia/commons/f/f4/Pulmonaryedema09.JPG License: CCBY-SA 3.0 Contributors: Own work Original artist: James Heilman, MD

13.3 Content license• Creative Commons Attribution-Share Alike 3.0